4 Acute Frontal Sinusitis

Contents

Introduction . . . . 33

Etiology and Pathophysiology of Acute Frontal Sinusitis . . . . 34

Uncomplicated Acute Frontal Sinusitis . . . . 34

Diagnosis . . . . 34

Bacteriology . . . . 35

Treatment . . . . 35

Complicated Acute Frontal Sinusitis . . . . 36

Diagnosis . . . . 36

Bacteriology . . . . 38

Treatment . . . . 39

Advantages and Disadvantages of Trephination . . 40 Advantages . . . . 40

Disadvantages . . . . 40

References . . . . 40

Introduction

Acute sinusitis is one of the leading diagnoses made in ambulatory medicine. The National Ambulatory Medical Care Survey (NAMCS) estimates that 20 mil- lion cases of acute bacterial rhinosinusitis (ABRS) occur each year [1]. The incidence of acute frontal si- nusitis (AFS) specifically is considerably lower, less common than maxillary sinusitis in adults and eth- moid sinusitis in children. Medical therapies for acute sinusitis result in expenditures of $3.5 billion per year in the United States. Of all antibiotics pre- scribed in 2002, 9% of pediatric prescriptions and 18% of adult prescriptions were written for a diagno- sis of acute sinusitis [1].

AFS occurs most commonly in adolescent males and young men. While the reasons for the male pred-

Core Messages

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with a viral upper respiratory tract infection.

Bacterial infection is suspected if symptoms are persistent for at least 10 days

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쐽

patients with uncomplicated AFS are Hemophilus influenza, Streptococcus pneu- moniae, and Moraxella catarrhalis

쐽

쐽

toms are protracted and severe

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쐽

쐽

쐽

Acute Frontal Sinusitis

Douglas Reh, Peter H. Hwang

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ic clinical consequences if not detected promptly.

Etiology and Pathophysiology of Acute Frontal Sinusitis

Acute frontal sinusitis is most commonly preceded by a viral upper respiratory tract infection. Human rhinovirus is implicated in 50% of cases, but other vi- ruses may include coronavirus, influenza, parain- fluenza, respiratory syncytial virus, adenovirus, and enterovirus. The peak prevalence of these viruses oc- curs in early fall and spring, which parallels the peak incidence of ABRS. Viruses upregulate pro-inflam- matory cytokines such as interleukin-1, interleukin- 6, interleukin-8, tumor necrosis factor-α, as well as other inflammatory mediators such as histamine and bradykinin. Viruses also suppress neutrophil, macro- phage, and lymphocyte function and can thereby in- hibit the immune response [2]. The viral induction of the inflammatory cascade results in acute mucosal edema, occlusion of sinus ostia, and impaired muco- ciliary clearance. Mucus stasis can then favor the pro- liferation of pathogenic micro-organisms, resulting in acute bacterial sinusitis. Other risk factors for acute sinusitis include a variety of host factors: septal deviation, nasal polyposis, and immunodeficien- cy/immunosuppression, among others.

While acute sinusitis typically affects the ethmoid and maxillary sinuses, progression of disease to in- volve the frontal sinus may be influenced by anatom- ic variations of the frontal sinus. The frontal sinus be- gins developing at age 3. Four frontal pits along the upper lateral wall of the embryological middle mea- tus differentiate into the anterior ethmoid cells. The second of these furrows evaginates from the anterior ethmoid region into the frontal bone, creating the frontal sinus [3]. Because the frontal sinus is embryo- logically derived from pneumatization of the eth- moid, frontal sinus outflow is thus influenced and de- fined by the degree of pneumatization of the ethmoid labyrinth. A variety of ethmoid-derived structures that comprise the frontal recess can thus narrow the

Uncomplicated Acute Frontal Sinusitis

Diagnosis

AFS is principally a clinical diagnosis based on type and duration of symptoms. CT scans, when ordered to diagnose acute bacterial sinusitis, may yield false positives. Gwaltney et al. showed that 87% of adults with acute onset of upper respiratory tract infection (URI) symptoms demonstrate CT evidence of nasal cavity mucosal thickening and sinus opacification [4]. They also showed that after 2 weeks without anti- biotic therapy, repeat CT scans showed improvement in 79% of 14 patients with these findings. Sinus aspi- ration studies have shown that significant bacterial growth occurs in approximately 60% of patients with URI symptoms lasting for 10 days or more [5]. There- fore persistent or worsening symptoms after 10 days may indicate a bacterial infection [1].

In 1997 the American Academy of Otolaryngology- Head and Neck Surgery Foundation assembled the Rhinosinusitis Task Force (RSTF) to develop clinical definitions of rhinosinusitis. Rhinosinusitis as de- fined by the RSTF is “inflammation of the nasal cavity and paranasal sinus” [6]. The RSTF subclassified rhinosinusitis into three major clinical categories based on duration of symptoms: acute, with symp- toms lasting less than 4 weeks; subacute, between 4 and 12 weeks; and chronic, greater than 12 weeks.

By RSTF guidelines, patients with rhinosinusitis must meet a variety of symptomatic major and mi- nor criteria.

The major criteria defined by the RSTF include:

쐽 Facial pain or pressure

쐽 Nasal congestion

쐽 Nasal obstruction

쐽 Purulent rhinorrhea

쐽 Hyposmia or anosmia

쐽 Fever (for acute rhinosinusitis only)

쐽 Purulence on nasal exam

4

The minor criteria defined by the RSTF include:

쐽 Headache

쐽 Nonacute fever

쐽 Halitosis

쐽 Fatigue

쐽 Dental pain

쐽 Cough

쐽 Ear pain or pressure

A diagnosis of rhinosinusitis requires either two ma- jor factors, one major and two minor factors, or pu- rulence in the nasal cavity on physical exam [6].

There are no site-specific criteria for the diagnosis of AFS. Generally frontal sinus symptoms are local- ized to the brow, temple, and frontal bone region.

Frontal headache is the most prevalent symptom of AFS [7]. Thus, a diagnosis of AFS should be consid- ered in patients who meet RSTF criteria for acute si- nusitis, in whom symptoms localize to the forehead region. In some cases, the acute onset of frontal head- ache, even in the absence of more classic symptoms such as nasal congestion and rhinorrhea, should prompt the physician to consider a diagnosis of AFS.

This is especially true in those patients without a his- tory of chronic headache.

Although most cases of acute rhinosinusitis can be diagnosed by symptoms alone, the physical exam- ination can provide helpful adjunctive diagnostic in- formation. Transillumination and palpation, while classically described for physical exam of the sinuses, are relatively nonspecific tests. Anterior rhinoscopy and nasal endoscopy, however, can be useful adjunc- tive diagnostic tools. Examination of the nasal cavity may reveal mucosal edema, purulent discharge, or anatomic obstructions such as septal deviation or polyposis. Purulent secretions may be aspirated under endoscopic visualization and cultured to guide antimicrobial therapy. During aspiration and culture, the endoscope should be used to retract the nasal vestibule away to minimize contamination of the culture device by normal nasal vestibular flora.

Unless a complication of acute sinusitis is suspect- ed, imaging studies such as CT and MRI are not nec- essary in making the diagnosis of AFS.

Bacteriology

While the bacteriology of acute maxillary sinusitis has been well documented by maxillary tap studies, the bacteriology of AFS has not been well studied.

Data are limited principally because of the difficulty of accessing the frontal sinus for cultures. Brook ob- tained aspirates from the frontal sinuses of 15 patients with acute infection [8]. Twenty isolates were grown from 13 of the specimens. The predominant aerobic and facultative organisms were Haemophilus influen- zae (6/13), Streptococcus pneumoniae (5), and Morax- ella catarrhalis (3). B-lactamase producing organisms were isolated in 33% of the specimens. Limitations of this study were its small numbers and the lack of doc- umentation of sampling technique.

Given that AFS typically occurs in conjunction with acute maxillary and ethmoid sinusitis, it seems reasonable to extrapolate data for acute maxillary si- nusitis to that for AFS. Indeed, the organisms cul- tured in the Brook study did parallel those obtained from the maxillary sinuses in other studies; namely, Streptococcus pneumoniae, Haemophilus influenzae and Moraxella catarrhalis [1].

Treatment

The goals of treating uncomplicated AFS are:

쐽 to control the infectious component of the disease process using antimicrobial therapy

쐽 to reduce the edematous, obstructive compo- nent of the disease process and restore sinus patency using decongestant therapy

쐽 Uncomplicated AFS is almost exclusively treated medically; surgical therapy is rarely indicated.

Antibiotic therapy should be selected for coverage of the primary organisms associated with acute rhino- sinusitis: S. pneumoniae, H. influenzae, and M. catar- rhalis. Drug resistance has become an increasing concern in the treatment of ABRS. Since the early 1990’s, the rates of penicillin resistance in S. pneu- moniae have increased dramatically, with 15% of iso-

lates showing intermediate resistance and 25% show- ing high resistance. Macrolide- (18%) and trimetho- prim/sulfamethoxazole (TMP/SMX) (20%)-resistant strains of S. pneumoniae are also significant in the United States [9]. Thirty percent of H. influenzae and greater than 95% of M. catarrhalis cultured are B-lac- tamase-producing isolates [1]. Resistance patterns and prevalence differ by geographic region. Table 4.1 shows differences in bacterial resistance by U.S. re- gion [10].

The Sinus and Allergy Health Partnership recently published antibiotic recommendations for the treat- ment of mild to moderate ABRS. These recommen- dations are based on clinical efficacy and reflect drug

and consideration should be given to endoscopic ex- am and culture.

Adjunctive medical treatment in AFS is aimed pri- marily at re-establishing the patency of the frontal recess and ostiomeatal complex through which the frontal sinus drains. Topical (oxymetazoline, pheny- lephrine) and oral (pseudoephedrine) decongestants and mucolytics (guaifenesin) may improve drainage of the affected sinuses. Selected patients with known inflammatory dysregulation, such as those with atop- ic disease, aspirin sensitivity, or nasal polyposis may benefit from oral steroids. When used in carefully se- lected patients, steroids can acutely reduce inflam- mation and facilitate drainage of affected sinuses [11].

Complicated Acute Frontal Sinusitis

Diagnosis

Occasionally, patients with AFS may present in acute distress with toxic clinical features. Clinical findings such as prostration, severe headache, or orbital com- plaints should raise suspicion for an infectious com- plication of AFS.

Complications from AFS principally involve:

쐽 extension to intracranial structures

쐽 the orbits may occasionally be affected

Although the true incidence of AFS-related compli- cations is unknown, a study of 649 patients admitted to the hospital for sinusitis showed an intracranial complication rate of 3.7% [12].

The frontal sinus is susceptible to extrasinus spread of infection in part because its venous drain- age occurs through diploic veins that traverse the posterior table and communicate with the venous supply of the meninges, cavernous sinus and dural si- nuses. These venous channels may be more porous in the developing sinus, and thus adolescents and young

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West

San Diego, CA 30 10.0 23.30

Los Angeles, CA 51 5.9 15.70

San Francisco, CA 52 9.6 23.10

Portland, OR 22 22.7 31.80

Seattle, WA 50 18.0 18.00

Denver, CO 51 21.6 13.70

Salt Lake City, UT 50 16.0 16.00

Phoenix, AZ 59 10.2 35.60

Midwest

Iowa City, IA 54 11.1 16.70

Indianapolis, IN 56 10.7 19.60

Chicago, IL 41 14.6 12.20

Milwaukee, WI 53 11.3 32.10

Detroit, MI 58 8.6 5.20

Cleveland, OH 52 7.7 34.60

East

Rochester, NY 50 18.0 22.00

Boston, MA 31 6.5 19.40

New York, NY 59 15.3 20.30

Philadelphia, PA 52 19.2 7.70

Washington DC 20 5.0 35.00

South

Chapel Hill, NC 41 9.8 56.10

Mobile, AL 49 10.2 16.30

Houston, TX 55 20.0 38.20

Dallas, TX 44 11.4 15.90

Miami Beach, FL 21 19.1 28.60

From [10]

adults (especially male) are at increased risk for com- plications of AFS.

Suspicion for complicated AFS should be elevated when:

쐽 Symptoms are protracted or more severe than would be expected for a typical case of acute sinusitis

쐽 On physical examination, there is periorbital edema or discoloration, which can indicate a preseptal cellulitis, or painful or restricted eye movement, which may indicate an orbital cel- lulites or abscess

쐽 Neurologic findings such as altered mental status, seizure, or cranial neuropathy are present, which may indicate intracerebral complications

As in uncomplicated AFS, nasal endoscopy may yield cultures of purulent material that can guide antimi- crobial therapy. Lumbar puncture may also be indi- cated to obtain CSF cultures and to rule out meningi- tis. Consultations with an ophthalmologist, neuro- surgeon, neurologist, or infectious disease specialist should be considered.

In contrast to uncomplicated AFS, radiologic studies play an important role in confirming and characteriz- ing the extent of extrasinus infectious involvement. CT scan is the imaging modality of choice in evaluating intracranial or orbital complications of AFS. Studies should be performed with IV contrast in axial and cor- onal planes. With bone and soft tissue algorithms, CT scans can characterize bony erosions of the frontal si- nus as well as phlegmons or fluid collections in adja- cent orbital and intracranial soft tissue. Serial imaging studies should be considered in patients who appear clinically unresponsive to initial treatment.

Table 4.2.Recommended antibiotic therapy for adults with mild or moderate ABRS

Initial therapy Calculated Calculated Switch therapy options clinical bacteriologic (no improvement after 72 hours) efficacy (%) efficacy (%)

Mild disease with no recent antimicrobial use in past 4–6 weeks

Amoxicillin/clavulanate (1.75–4 g/250 mg/d) 90–91 97–99

Amoxicillin (1.5–4 g/d) 87–88 91–92 Gatifloxacin/levofloxacin/moxifloxacin

Cefpodoxime proxetil 87 91 Amoxicillin/clavulanate (4 g/250 mg)

Cefuroxime axetil 85 87 Ceftriaxone

Cefdinir 83 85 Combination therapy

B-Lactam Allergic

TMP/SMX 83 84

Doxycycline 81 80 Gatifloxacin/levofloxacin/moxifloxacin

Azithromycin/erythromycin/clarithromycin 77 73 Rifampin plus clindamycin Mild disease with recent antimicrobial

use in past 4–6 weeks or moderate disease

Gatifloxacin/levofloxacin/moxifloxacin 92 100

Amoxicillin/clavulanate (4 g/250 mg) 91 99 Reevaluate patient

Ceftriaxone 91 99

B-Lactam Allergic

Gatifloxacin/levofloxacin/moxifloxacin 92 100 Reevaluate patient

Clindamycin and rifampin From [1]

symptom, although subsequently there may be a quiescent asymptomatic phase during which an ab- scess has coalesced [13]. Overall mortality reported in the literature ranges widely from 0% to 53%

[13,14].

Meningitis is another important neurologic com- plication of AFS [12].

Symptoms suggestive of meningitis include:

쐽 High fever

쐽 Photophobia

쐽 Neck pain or stiffness

쐽 Severe headache

쐽 Mental status changes

Mortality is reported as high as 45% [15]. While men- ingitis is the second most common intracranial com- plication of acute sinusitis in general, the frontal si- nus as a site of origin is less common than the sphe- noid (most common) and the ethmoid sinuses. Ad- vanced cases of frontal sinusitis with meningitis may also be associated with subdural or epidural abscess- es.When these abscesses occur they typically develop immediately posterior to the frontal sinus along pathways of venous drainage [14].

Osteomyelitis of the frontal sinus may be caused by direct extension of infection or by thrombophle- bitis of the diploic veins. Of all the paranasal sinuses, the frontal sinus is most commonly associated with osteomyelitis. When osteomyelitis involves the ante- rior table, a subperiosteal abscess may develop, pre- senting as a subcutaneous fluctuant protuberance over the brow or forehead. This abscess is known as Pott’s Puffy Tumour, which was first described by Sir Percival Pott in 1775 [16]. Strictly an infectious com- plication and not neoplastic in any way, Pott’s Puffy Tumour may present with severe headache, fever, and photophobia.

Cavernous sinus thrombosis and superior sagittal sinus thrombosis comprise another important class of complications associated with AFS.

쐽 Trigeminal nerve (V2 and V3) deficits

Early clinical recognition is important, as symptoms can quickly progress, and mortality exceeds 30%

[17–19]. Superior sagittal sinus thrombosis is asso- ciated with subdural abscess and has a high mortality rate, 80% [18].

Isolated AFS rarely causes orbital complications.

However, AFS in the context of pansinusitis is asso- ciated with 60–80% of orbital complications [20,21].

Although direct spread to the orbits from the frontal sinus is possible, the ethmoid sinuses are more com- monly implicated in the development of orbital com- plications.

Bacteriology

The organisms cultured from the sinuses of patients with intracranial abscesses include [12]:

쐽 Staphylococcus aureus

쐽 Anaerobic streptococci

쐽 Streptococcus epidermidis

쐽 Streptococcus pneumoniae

쐽 Staphylococcus intermedius

쐽 Beta-hemolytic streptococci

쐽 Gram-positive aerobes and anaerobes are the predominant bacteria in complicated AFS

Table 4.3 summarizes the organisms cultured from paranasal sinuses in patients with intracranial com- plications [12]. Table 4.4 shows Goldberg et al.’s sum- marization of the common organisms associated with AFS complications and the recommended pri- mary antibiotic therapy based on the Sanford Guide to Antimicrobial Treatment [14].

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Treatment

Treatment of complicated AFS includes aggressive medical therapy and surgery to drain both the in- volved sinus and the abscess collection if present.

Because of the acuity and morbidity of complicat- ed frontal sinusitis, patients should be admitted for

intravenous antibiotic therapy, serial neurologic ex- amination, and intravenous hydration. Empiric anti- biotic therapy should be initiated immediately, choosing broad-spectrum agents that have favorable penetration of the blood-brain barrier. If cultures can be obtained, antibiotic therapy may be tailored accordingly. It should be noted that a significant per- centage of cultures from patients with intracranial complications are negative. This may perhaps occur because antibiotic therapy is often initiated emer- gently before cultures can be obtained. Antila et al.

obtained 103 frontal sinus cultures in patients with AFS and simultaneous maxillary sinusitis [22]. Only 30% of these cultures were positive for bacteria.

Twenty-one percent of the cultures in Clayman et al.’s study were negative [12]. In such cases, bacteriologic data from historical cohorts may be used to guide antibiotic selection.

Depending on the degree of morbidity, many pa- tients will require continuation of intravenous anti- biotic therapy as an outpatient after resolution of the acute phase of illness. Oral antibiotic therapy may be appropriate in selected patients. Duration of treat- ment varies with the nature and severity of the com- plication, as well as the response to initial therapy.

The use of intravenous corticosteroids in patients with AFS complications is controversial. Some stud-

Table 4.3.Organisms cultured from paranasal sinuses with as- sociated intracranial complications

Organism n (%)

Negative cultures 5 (21)

S. aureus 5 (21)

Anaerobic streptococci 3 (12)

S. epidermidis 2 (8)

S. pneumoniae 2 (8)

S. intermedius 2 (8)

b-Hemolytic streptococci 2 (8)

S. viridans 1 (4)

Actinomycoses sp. 1 (4)

Fusobacterium necrosporum 1 (4) Bacteroides melaninogenicus 1 (4) From [12]

Table 4.4.Common organisms associated with ABRS-related complications and recommended empiric antibiotic therapy Disease Most common organism Primary drug choice Alternative 1 Pott’s tumor (acute S. aureus, streptococci, Pencillinase-resistant Third-generation osteomyelitis) anaerobes, polymicrobial penicillin and metronidazole, cephalosporin and

consider vancomycin vancomycin and metronidazole Intracranial abscess Streptococci, Bacteroides sp. 3^rdgeneration cephalosporin High-dose PCN G

and metronidazole and metronidazole Orbital complication S. pneumococcus,H. influenzae, 2^ndand 3^rdgeneration Ticarcillin/ clavulanate

M. catarhalis, S. aureus cephalosporin or ampicillin/ or piperacillin and

sulbactam tazobactam

Meningitis S. pneumococcus, 3^rdgeneration cephalosporin Meropenem and

H. influenzae and vancomycin vancomycin

Dural sinus thrombophlebitis S. aureus, group A Pencillinase-resistant Imipenem or meropenem streptococcus, H. influenzae, penicillin and 3^rdgeneration and vancomycin

fungal organisms cephalosporin

From [14]

steroids improve mortality or morbidity associated with cerebral edema; thus the use of corticosteroids should be considered on an individual basis.

Treatment of complicated AFS often involves sur- gery in addition to antibiotic therapy. Patients with intracranial abscesses may require neurosurgical drainage concurrently with surgical treatment of the frontal sinus.

Methods of draining the frontal sinus include:

쐽 Trephination

쐽 Endoscopic frontal sinusotomy

쐽 External ethmoidectomy

Advantages and Disadvantages of Trephination

Advantages

쐽 Technical simplicity

쐽 Efficacy of draining the sinus

쐽 Access to the sinus lumen for irrigation

Disadvantages 쐽 Scar

쐽 Potential injury to the supraorbital nerve 쐽 The critical area of impaired outflow of the

sinus is not addressed

In experienced hands, endoscopic frontal sinusoto- my may be an alternative surgical technique in com- plicated AFS. The endoscopic approach provides a minimally invasive means of draining the sinus and anatomically improving frontal outflow. Disadvan- tages of the endoscopic approach include its techni-

30% of cases) and frontal stenosis [24].

References

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